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机构地区:[1]西安交通大学医学院生理与病理生理学系,西安710061
出 处:《生理学报》2008年第2期270-274,共5页Acta Physiologica Sinica
基 金:the National Natural Science Foundation of China(No.30170310)
摘 要:前期研究显示低频率多串刺激能够在成年大鼠海马CA1区诱发稳定的长时程压抑(long-term depression,LTD),而这种LTD的受体机制目前还不清楚。本研究采用成年大鼠海马脑片标本,电刺激Schaffer侧枝传入纤维,在CA1区锥体细胞层记录群体锋电位(population spikes,PS),并分别应用N-甲基-D-天冬氨酸(N-methyl-D-aspartate,NMDA)受体和代谢型谷氨酸(metabotropic glutamate,mGlu)受体的拮抗剂AP5和MCPG,观察两组低频率(2-Hz和5-Hz)多串刺激能否诱导LTD,以揭示不同刺激形式诱导成年大鼠LTD的可能受体机制。结果显示,AP5和MCPG都能抑制由2-Hz多串刺激诱导的LTD:强直刺激后20min时PS幅度分别为基础值的(96.0±3.5)%(n=10)和(95.7±4.1)%(n=8)。MCPG能够抑制5-Hz多串刺激诱导的LTD的产生,而AP5不能:分别应用AP5和MCPG后,强直刺激后35min时PS的幅度分别为基础值的(73.6±4.4)%(n=10)和(98.2±8.9)%(n=8)。以上结果提示,2-Hz多串刺激诱导的LTD可能依赖于NMDA受体与mGlu受体的共同活化,而5-Hz多串刺激诱导的LTD只与mGlu受体有关。因此,不同频率的多串刺激诱导的LTD涉及不同的谷氨酸受体机制。Previous reports suggested that a novel stimulus pattern of multi-train stimulus at low-frequency (2-Hz or 5-Hz) could induce stable long-term depression (LTD) in the CA1 area of adult rat hippocampus. In the present study, in order to determine the mechanism in LTD induced by the two novel tetanus patterns, changes in the population spikes (PS) in the hippocampal CA1 area of adult rats following the multi-train stimulus in the presence of AP5 [antagonist of N-methyl-D-aspartate receptors (NMDARs)] or MCPG [antagonist of type Ⅰ/Ⅱ metabotropic glutamate receptors (mGluRs)] were recorded. The results showed that both AP5 and MCPG inhibited the LTD induced by 2-Hz multi-train stimulus. The mean amplitude of population spikes (PSA) normalized to the baseline was (96.0±3.5)% after applying AP5 (n=10) and (95.7±4.1)% after applying MCPG (a=8), respectively, measured at 20 rain post-tetanus. While 5-Hz multi-train tetanus failed to induce LTD in the presence of MCPG. The mean PSA was (73.6±4.4)% (n=10) and (98.2±8.9)% (n=8) in the presence of AP5 and MCPG, respectively, measured at 35 min post-tetanus. So it is suggested that LTD induced by 2-Hz multi-train tetanus involves co-activation of NMDARs and mGluRs, while LTD induced by 5-Hz multi-train tetanus is only related to activation of mGluRs.
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